Shoichi Nishise ¹, Yuji Takeda ², Hidetoshi Nara ², Yasuhiko Abe ¹, Yu Sasaki ¹, Hironobu Asao ², Yoshiyuki Ueno ¹ , Ther Apher Dial. 2018 Jun;22(3):261-265.

These results suggest that independent of incubation temperature, sICAM-1 and sVCAM-1 are likely to adsorb CA beads. These molecules may be a new index for predicting the therapeutic effects of GMA.

https://pubmed.ncbi.nlm.nih.gov/29745046/

Shuai Ma ¹, Qingqing Xu ¹, Bo Deng ¹, Yin Zheng ², Hongyan Tian ¹, Li Wang ³, Feng Ding ⁴ , Intensive Care Med Exp. 2017 Dec;5(1):18.

This study showed that selective granulocyte and monocyte adsorption with cellulose acetate beads might ameliorate cecal ligation and puncture (CLP)-induced sepsis and improve survival and organ function.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5366986/pdf/40635_2017_Article_129.pdf

https://pubmed.ncbi.nlm.nih.gov/28342161/

Shoichi Nishise ¹, Yasuhiko Abe ¹, Eiki Nomura ², Takeshi Sato ¹, Yu Sasaki ¹, Daisuke Iwano ¹, Kazuya Yoshizawa ¹, Makoto Yagi ¹, Kazuhiro Sakuta ¹, Yoshiyuki Ueno ¹ , Ther Apher Dial. 2016 Aug;20(4):354-9.

 In conclusion, CA beads inhibited IL-23 release from adsorbed GMs. The biological effects of this decrease in IL-23 release during GM adsorption to CA beads need further clarification.

https://pubmed.ncbi.nlm.nih.gov/27523075/

Shoichi Nishise ¹, Yasuhiko Abe ¹, Eiki Nomura ¹, Takeshi Sato ¹, Yu Sasaki ¹, Daisuke Iwano ¹, Makoto Yagi ¹, Kazuhiro Sakuta ¹, Rika Shibuya ¹, Naoko Mizumoto ¹, Nana Kanno ¹, Yoshiyuki Ueno ¹ , Ther Apher Dial. 2015 Aug;19(4):330-5.

In conclusion, CA beads inhibited the release of TGF-β from adsorbed platelets. The biological effects of this reduction of TGF-β release during platelet adsorption to CA beads need further clarification.

https://pubmed.ncbi.nlm.nih.gov/26386220/

C D’Arrigo ¹, J J Candal-Couto, M Greer, D J Veale, J M Woof Clin Exp Immunol 1995 Apr;100(1):173-9. doi: 10.1111/j.1365-2249.1995.tb03620.x.

Human polymorphonuclear cells (PMN) were found to adhere to a novel model of blood vessel wall-associated IgG. The internal surfaces of cellulose acetate hollow fibres, of comparable internal diameter to small blood vessels, were coated with normal serum human IgG, heat-aggregated IgG (HAIgG), laminin or fibrinogen. Under conditions of flow mimicking those in a small vessel, PMN were found to adhere markedly only to immunoglobulin-coated fibres. Arrest on HAIgG was inhibited by excess soluble IgG but not by bovine serum albumin (BSA), demonstrating that the adhesion was IgG-specific and presumably mediated by Fc gamma R on the PMN surface. Pre-adsorption of serum components onto HAIgG-coated fibres enhanced PMN arrest, due most probably to fixation of complement components by immobilized HAIgG, resulting in additional potential to entrap PMN via complement receptors such as CR3. Treatment of PMN with the regulatory neuropeptide substance P also enhanced adhesion to HAIgG-coated fibres and caused increased surface expression of Fc gamma RI, Fc gamma RII and Fc gamma RIII. A mouse cell line derived from L cells, hR4C6, stably transfected with human Fc gamma RII, was found to adhere under flow to HAIgG-coated fibres, whilst untransfected parent L cells did not. This adhesion was similarly inhibited by excess soluble IgG, confirming the capability of Fc gamma R to mediate cell arrest. The study strongly suggests that Fc gamma R may play an important role in intravascular PMN arrest and we speculate that in inflammatory diseases PMN may adhere via Fc gamma R to immobilized immunoglobulin on the vascular endothelium, with subsequent degranulation and tissue damage.

https://pubmed.ncbi.nlm.nih.gov/7535210/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534271/